本文選題：尿毒癥毒素 + 危險信號相關(guān)分子模式��； 參考：《山西醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:研究某些內(nèi)源性代謝產(chǎn)物在慢性腎臟病患者體內(nèi)濃度升高的機(jī)制,以及這些內(nèi)源性代謝產(chǎn)物是否可以激活危險信號相關(guān)分子模式受體,誘導(dǎo)炎癥發(fā)生,并進(jìn)一步分析這些內(nèi)源性代謝產(chǎn)物的調(diào)控機(jī)制。方法:在代謝產(chǎn)物以及基因數(shù)據(jù)庫中,找到尿毒癥毒素受體及其關(guān)鍵合成酶與轉(zhuǎn)化酶的編碼基因。在NIH-Geo數(shù)據(jù)庫中找到代謝性疾病及炎癥通路相關(guān)的13個微陣列數(shù)據(jù)庫,使用GEO2R的分析方法分析尿毒癥毒素相關(guān)基因,選擇p?0.05的基因分析結(jié)果。結(jié)果:在慢性腎臟病中,小分子尿毒癥毒素種類占人體小分子代謝產(chǎn)物的1/80;尿毒癥毒素濃度不只在慢性腎臟病中升高,在其他疾病中也會升高;蛋白結(jié)合型尿毒癥毒素可以促進(jìn)或抑制炎癥因子的表達(dá);與代謝綜合征和2型糖尿病患者相比,慢性腎臟病患者腎小管及心血管疾病患者脂肪組織中尿毒癥毒素基因顯著升高;caspase-1通路和TNF-alpha通路明顯上調(diào)尿毒癥毒素基因表達(dá);調(diào)節(jié)性T細(xì)胞顯著下調(diào)尿毒癥毒素基因的表達(dá)。游離性尿毒癥毒素中,20%促進(jìn)炎癥反應(yīng),12%抑制炎癥反應(yīng);蛋白結(jié)合型尿毒癥毒素中,14%促進(jìn)炎癥反應(yīng),5%抑制炎癥反應(yīng);在尿毒癥相關(guān)代謝性疾病中,19.52%尿毒癥毒素相關(guān)基因表達(dá)上調(diào),33.14%尿毒癥毒素相關(guān)基因表達(dá)下調(diào)。結(jié)論:尿毒癥毒素由于腎臟濾過功能衰竭而被動積累,并且在慢性腎臟病中選擇性濃度升高。尿毒癥毒素可以作為危險或穩(wěn)態(tài)相關(guān)分子模式調(diào)控炎癥反應(yīng),其調(diào)控途徑為包括caspase-1通路在內(nèi)的炎癥因子通路。
[Abstract]:Aim: to investigate the mechanism of elevated concentrations of some endogenous metabolites in patients with chronic kidney disease and whether these endogenous metabolites can activate risk signal-related molecular model receptors and induce inflammation. The regulation mechanism of these endogenous metabolites was further analyzed. Methods: the genes encoding uremic toxin receptors and their key synthase and invertase were found in metabolites and gene databases. Thirteen microarray databases related to metabolic diseases and inflammatory pathways were found in NIH-Geo database. The analysis method of GEO2R was used to analyze uremic toxin-related genes, and the results of p0.05 gene analysis were selected. Results: in chronic kidney disease, the type of small molecule uremic toxin accounted for 1 / 80 of human small molecule metabolites, the concentration of uremic toxin increased not only in chronic kidney disease, but also in other diseases. Protein-binding uremic toxins can promote or inhibit the expression of inflammatory factors in patients with metabolic syndrome and type 2 diabetes. Uremic toxin gene increased significantly in renal tubules and adipose tissue of patients with chronic kidney disease and TNF-alpha pathway upregulated the expression of uremic toxin gene, and regulatory T cells significantly down-regulated the expression of uremic toxin gene. 20% of free uremic toxins promoted the inflammatory response and 12% inhibited the inflammatory response, while 14% of the protein-binding uremic toxins promoted the inflammatory response and 5% of the protein-binding uremic toxins inhibited the inflammatory response. In uremic related metabolic diseases, 19.52% of uremic toxin-associated genes were up-regulated and 33.14% of uremic toxin-associated genes were down-regulated. Conclusion: uremic toxin accumulates passively because of renal filtration failure, and the selective concentration in chronic kidney disease is increased. Uremic toxin can be used as a dangerous or homeostasis related molecular model to regulate inflammatory response, and its regulatory pathway is the inflammatory factor pathway, including the caspase-1 pathway.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R692.5

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